Loss of SNAI2 in Prostate Cancer Correlates With Clinical Response to Androgen Deprivation Therapy
Author(s) -
Marek Cmero,
Natalie J. Kurganovs,
Ryan Stuchbery,
Patrick J. McCoy,
Corrina Grima,
Anne Ngyuen,
Ken Chow,
Stefano Mangiola,
Geoff Macintyre,
Nicholas Howard,
Michael Kerger,
Philip Dundee,
Paul Ruljancich,
David C. Clarke,
Jeremy Grummet,
Justin S. Peters,
Anthony J. Costello,
Sam Norden,
Anthony J. Ryan,
Phillip Parente,
Christopher M. Hovens,
Niall M. Corcoran
Publication year - 2021
Publication title -
jco precision oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.405
H-Index - 22
ISSN - 2473-4284
DOI - 10.1200/po.20.00337
Subject(s) - prostate cancer , androgen deprivation therapy , regulator , androgen receptor , bicalutamide , reprogramming , cancer research , medicine , epithelial–mesenchymal transition , oncology , downregulation and upregulation , androgen , cancer , biology , cell , metastasis , gene , genetics , hormone
Androgen receptor (AR) signaling is important in prostate cancer progression, and therapies that target this pathway have been the mainstay of treatment for advanced disease for over 70 years. Tumors eventually progress despite castration through a number of well-characterized mechanisms; however, little is known about what determines the magnitude of response to short-term pathway inhibition.
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